Secondary hypertension mnemonic
A simple mnemonic for recalling the causes of secondary hypertension is CHARPLES. It is worth noting that most of the secondary causes of hypertension are of endocrine origin. Perturbations in each endocrine gland can contribute to secondary hypertension.
Causes of secondary hypertension
- C : Conn’s syndrome (primary hyperaldosteronism), Cushing’s syndrome, Congenital Adrenal Hyperplasia.
- H : Hyperparathyroidism, Hyperthyroidism
- A : Aortic coarctation, Adrenal carcinoma
- R : Renovascular hypertension, Reninoma, Renal parenchymal disease
- P : Pheochromocytoma
- L : Liddle’s syndrome, Licorice
- E : Estrogen pills (oral contraceptive pill)
- S : Sleep Apnea
The mechanism of secondary hypertension
What is pseudohyperaldosteronism?
These are endocrine conditions that present with some of the clinical features of primary hyperaldosteronism (hypertension and hypokalemia) but do not exhibit the expected increase in plasma aldosterone to plasma renin ratio. Patients with pseudohyperaldosteronism have low levels of both aldosterone and renin.
|Liddle’s syndrome||A gain-of-function mutation of the gene encoding the amiloride-sensitive epithelial sodium chloride transporter|
|Gordon syndrome (Familial hyperkalemic hypertension)||A gain of function mutation of the thiazide-sensitive sodium-chloride co-transporter in the distal nephron. Unlike other causes of pseudohyperaldosteronism, Gordon Syndrome is associated with hyperkalemia instead of hypokalemia.|
|Defects in adrenal steroidogenesis||Deficiency of 11beta-hydroxylase enzyme results in a build-up of 11-Deoxycorticosterone (which has intrinsic mineralocorticoid activity)|
|Cushing’s syndrome||Excess cortisol binds to the mineralocorticoid receptor due to saturation of the 11beta-hydroxysteroid dehydrogenase 2 enzyme. See cortisol to cortisone shunt|
|Congenital Apparent mineralocorticoid excess||An autosomal recessive condition characterized by an inactivating mutation of the 11beta-hydroxysteroid dehydrogenase 2 enzyme|
|Excessive intake of licorice, grapefruits or carbenoxolone. Medication induced apparent mineralocorticoid excess||Inhibition of 11beta-hydroxysteroid dehydrogenase 2. Glycyrrhizic acid inhibits 11beta-hydroxysteroid dehydrogenase 2 enzyme. Glycyrrhizic acid is present in the root of the licorice plant (Glycyrrhiza glabra).|
|Medication-induced||Corticosteroids and contraceptives|
|Congenital Adrenal Hyperplasia||11beta-hydroxylase and 17alpha-hydroxylase deficiency leads to a buildup of 11-Deoxycorticosterone (intrinsic mineralocorticoid activity)|
Armanini D, Calò L, Semplicini A. Pseudohyperaldosteronism: pathogenetic mechanisms. Crit Rev Clin Lab Sci. 2003 Jun;40(3):295-335.